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Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma

Alcohol is the one of the major causes of liver diseases and promotes liver cirrhosis and hepatocellular carcinoma (HCC). In hepatocytes, alcohol is converted to acetaldehyde, which causes hepatic steatosis, cellular apoptosis, endoplasmic reticulum stress, peroxidation, production of cytokines and...

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Autores principales: Sasaki-Tanaka, Reina, Ray, Ranjit, Moriyama, Mitsuhiko, Ray, Ratna B., Kanda, Tatsuo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9456124/
https://www.ncbi.nlm.nih.gov/pubmed/36077080
http://dx.doi.org/10.3390/ijms23179679
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author Sasaki-Tanaka, Reina
Ray, Ranjit
Moriyama, Mitsuhiko
Ray, Ratna B.
Kanda, Tatsuo
author_facet Sasaki-Tanaka, Reina
Ray, Ranjit
Moriyama, Mitsuhiko
Ray, Ratna B.
Kanda, Tatsuo
author_sort Sasaki-Tanaka, Reina
collection PubMed
description Alcohol is the one of the major causes of liver diseases and promotes liver cirrhosis and hepatocellular carcinoma (HCC). In hepatocytes, alcohol is converted to acetaldehyde, which causes hepatic steatosis, cellular apoptosis, endoplasmic reticulum stress, peroxidation, production of cytokines and reduces immune surveillance. Endotoxin and lipopolysaccharide produced from intestinal bacteria also enhance the production of cytokines. The development of hepatic fibrosis and the occurrence of HCC are induced by these alcohol metabolites. Several host genetic factors have recently been identified in this process. Here, we reviewed the molecular mechanism associated with HCC in alcoholic liver disease.
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spelling pubmed-94561242022-09-09 Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma Sasaki-Tanaka, Reina Ray, Ranjit Moriyama, Mitsuhiko Ray, Ratna B. Kanda, Tatsuo Int J Mol Sci Review Alcohol is the one of the major causes of liver diseases and promotes liver cirrhosis and hepatocellular carcinoma (HCC). In hepatocytes, alcohol is converted to acetaldehyde, which causes hepatic steatosis, cellular apoptosis, endoplasmic reticulum stress, peroxidation, production of cytokines and reduces immune surveillance. Endotoxin and lipopolysaccharide produced from intestinal bacteria also enhance the production of cytokines. The development of hepatic fibrosis and the occurrence of HCC are induced by these alcohol metabolites. Several host genetic factors have recently been identified in this process. Here, we reviewed the molecular mechanism associated with HCC in alcoholic liver disease. MDPI 2022-08-26 /pmc/articles/PMC9456124/ /pubmed/36077080 http://dx.doi.org/10.3390/ijms23179679 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Sasaki-Tanaka, Reina
Ray, Ranjit
Moriyama, Mitsuhiko
Ray, Ratna B.
Kanda, Tatsuo
Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma
title Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma
title_full Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma
title_fullStr Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma
title_full_unstemmed Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma
title_short Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma
title_sort molecular changes in relation to alcohol consumption and hepatocellular carcinoma
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9456124/
https://www.ncbi.nlm.nih.gov/pubmed/36077080
http://dx.doi.org/10.3390/ijms23179679
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